Sudden Infant Death Syndrome (SIDS), also called "Crib Death", can be defined as the sudden death of any infant which is unexpected according to history and in which a post-mortem fails to demonstrate an adequate cause of death. Although the death might be unexpected according to the infant's history as examined in a conventional manner a SIDS death might have been predictable or at least determined to be more probable with that specific infant due to its history. For example, premature infants, low birth weight infants and those with respiratory distress syndrome are more likely to suffer a SIDS death than other infants. Another group of infants more likely to be susceptible to a SIDS death would be the "Near-Miss" infants, i.e. those who have been successfully revived after respiration ceased. A number of other factors are known to be associated with an increased likelihood of suffering a SIDS death.
In an attempt to reduce the number of SIDS deaths, attempts have been made to identify those infants who would be more likely to suffer a SIDS death. After identifying such infants, the parents are notified and mechanical devices can be attached to the infant. These mechanical devices monitor the respiration and/or heartbeat of the infant and actuate an alarm when respiration and/or heartbeat ceases. The parents can respond to the alarm and revive the infant. Such devices are advantageous in that they do not require the administration of any drugs to the infant. However, they are undesirable in that they may fail due to mechanical malfunction or an interruption of their power supply. Further, individuals might fail to respond to the alarm or fail to respond fast enough in order to revive the infant. Perhaps most importantly, such devices do nothing to prevent respiratory arrest and respiratory arrest for even a short period of time can of course cause brain damage.
Due to the deficiencies with utilizing such systems and in an effort to advance science in this area a substantial number of studies have been done with respect to the mechanisms within the body controlling respiration. More specifically, studies have been done with respect to the causes for interrupting or depressing respiration. Recent studies have indicated that beta-endorphins cause depression of ventilatory regulation (CO.sub.2 -response test). (see Moss, I. R., and Freedman, E., Beta-Endorphins: "Effects on Respiratory Regulations". Life Science, 23:1271, 1978.) The study showed that these beta-endorphins depress the spontaneous discharge of respiratory center neurons and that the depressant effect on response to CO.sub.2 are temporarily reversed by the injection of naloxone. (Cdenavit-saubie, m.Champagnat, J., and Zieglgansberger, W: "Effects on opioids and Methionine-Enkephalin on pontine and Bulbar respiratory neurons of the cat". Brain res. 155:55, 1978.) The administration of naloxone invariably stimulates breathing in previously apneic subjects and also facilitates the breathing response to CO.sub.2 both by decreasing estimated CO.sub.2 threshold and increasing calculated fetal sensitivity to CO.sub.2. Naloxone is an opiate antagonist and thus the stimulation caused by administering naloxone is created by the displacement of endogenous opioids from their natural receptor sights. Thus the administration of naloxone blocks the action of endorphins which participate in the physiological suppression of respiratory control in fetal life.
Although naloxone can be useful in blocking endogenous endorphins and thus aid in the prevention of respiratory suppression or arrest, naloxone has a relatively short half-life and is substantially metabilized on the first pass through the liver. Due to its relatively short half-life (approximately 35-45 minutes) the drug must be administered frequently in order to have a continuous effect on preventing respiratory suppression or arrest. Since the drug is substantially metabolized on the first pass through the liver to a metabolite which is ineffective with respect to blocking endogenous endorphins, the drug can not generally be effectively administered via the GI tract. The need for frequent re-dosing and intravenous administration makes the use of naloxone in preventing SIDS impractical.